This invention relates to cardiac stimulating devices and particularly to implantable cardiac stimulating devices that deliver therapeutic shocks to cardiac tissue to interrupt pathological cardiac arrhythmias. More particularly, this invention is directed to a system and method for increasing the energy content of a therapeutic cardioversion or defibrillation shock as a function of any time delay from the initial onset of an arrhythmia to the time treatment will be administered.
The typical adult sinus rhythm range is between about 65 and about 85 heartbeats per minute (bpm). Generally, rates between 60 and 100 bpm are not a cause for concern. This range is referred to as the normal sinus rate range. Rates falling outside the sinus rate range are known as arrhythmias. An arrhythmia in which the sinus rate is above 100 bpm is called a tachycardia. An arrhythmia in which the sinus rate is below 60 bpm is called a bradycardia.
Common ventricular arrhythmias include ventricular tachycardia (VT) and ventricular fibrillation (VF). Ventricular arrhythmias are generally considered to be of greater concern than other types of arrhythmias due to the resultant loss of a substantial amount of cardiac output.
VT is a condition where an abnormally high ventricular heart rate severely affects the ability of the heart to pump blood. VT may result in a loss of consciousness due to a decrease in cardiac output. Sustained episodes of VT are particularly dangerous because they may deteriorate into VF.
VF is the most life threatening arrhythmia. VF is the result of rapid and disordered stimulation of the ventricles which prevents them from contracting in a coordinated fashion. This results in a severe drop in cardiac output as the pumping ability of the ventricles is compromised. VF leads to tissue narcosis due to the lack of an oxygenated blood supply and may result in the death of the individual within minutes if left untreated. An effective method of terminating VF is internal or external defibrillation, using a high energy electrical shock provided by an implantable or external defibrillator.
Defibrillators are a species of cardioverters. In contrast to pacemakers, cardioverters deliver a relatively high energy shock to the myocardial tissue. Among cardioverters, defibrillators administer shocks having the greatest energy content. Both cardioverters and defibrillators discharge a relatively large electrical shock across the heart in order to simultaneously depolarize all myocardial tissue. This allows the heart's SA node, which has the fastest spontaneous discharge cells and acts as the heart's natural pacemaker, to regain pacing control and return the heart to within the normal sinus rhythm range. While cardioversion is used for tachycardias of varying rates and severity, defibrillation is only used when the heart is fibrillating.
Generally, during cardioversion, a therapeutic electrical charge is delivered at about the same time a QRS complex occurs--to prevent the possibility of aggravating a tachycardia by either accelerating its frequency or by inducing the heart into ventricular fibrillation. Therapeutic cardioversion energies have a wide range--typically from about 0.05 joules to about 10 joules. During fibrillation the heart quivers instead of beats. Thus, defibrillation shocks, in contrast to cardioversion shocks, cannot be synchronized with a QRS complex because the QRS complexes are not discernable. Typical defibrillation energies range from about 5 joules to about 40 joules. It is desirable to expose the patient to the least amount of energy and the least number of shocks while maintaining a high probability of terminating the arrhythmia.
The lack of a suitable energy source was a major impediment to the development of modern implantable cardiac devices and particularly cardioverter-defibrillators. Initially, mercury zinc and later lithium iodine cells were used, but they were unable to provide the peak current requirements for cardioverter-defibrillators, which typically are in the range from about one to about two amperes for approximately 10 seconds. Lithium vanadium pentoxide batteries were able to meet this requirement, but had a characteristic precipitous voltage decline towards the end of their useable life. These batteries were abandoned because of the difficulty in accurately determining the remaining life of the battery. Currently, lithium silver vanadium pentoxide cells are favored for two reasons: (1) they have greater energy density (i.e., more milliampere-hours stored per unit of battery volume combined with a lower internal resistance); and (2) they have a gradual voltage decline over their usable life. The latter characteristic allows for a more accurate prediction of when the battery's useable life is near its end. However, as will be discussed below, because battery voltage declines with use and time, the time needed to develop high voltage across a capacitor increases as the battery ages. This principle is true for all types of batteries since all batteries suffer from that same limitation--namely, that available energy invariably decreases with time and usage.
Because the cardioversion or defibrillation voltage required is higher than available battery voltages, which are typically on the order of 6.4 volts (two 3.2 volt cells in series), a DC/DC converter is typically used to develop high voltages. The DC/DC oscillator takes the battery voltage and produces a high frequency pulsed voltage substantially equal in magnitude to the battery voltage. This high frequency pulsed voltage is converted by the DC/DC converter to high voltage typically by using a "step-up" transformer. This high frequency, high voltage is then full-wave rectified. The rectified voltage is applied to a pair of high voltage capacitors which charge incrementally with each rectified voltage pulse. Double anode aluminum electrolytic capacitors are typically used in modern cardiac devices.
When an implantable cardiac device senses fibrillation, a finite amount of time is required to charge the capacitors to their target voltage which can be preselected by a physician. The charge time of the capacitors is dependent upon any remaining charge from a previous high voltage therapy event or capacitor reformation, the battery current and voltage, and the combined capacitance of the capacitors. As a consequence, when battery voltage or current output decreases, it takes longer to develop the desired target voltage on the capacitors. This directly translates to a longer time-to-therapy because the cardioverter-defibrillator waits for the capacitor to charge to the target voltage before delivering the shock. Typically, at least two capacitors are used in series to facilitate higher energy storage for monophasic and biphasic pulses of varying waveforms and to allow for administering of sequential pulses, as well as to ensure that sequential pulses are of the same amplitude.
Among the latest improvements in implantable cardiac stimulating devices are tiered therapy systems. These systems typically allow for the administration by a single device of anti-tachycardia pacing therapy in addition to cardioversion and defibrillation therapies. U.S. Pat. No. 4,830,006 issued May 16, 1989 to Haluska et al. describes such a device. These systems can be programmed to administer a number of consecutive cardioversion or defibrillation therapies with each subsequent therapy having an increased level of aggressiveness. When the initial therapy has little or no therapeutic effect, therapy is re-administered. Each time therapy is re-administered, the device may need to cycle through the sensing, charging and delivery cycle. The time delay due to past failed therapy applications can be extensive.
Time-to-therapy can be a determining factor in the efficacy of a therapeutic shock. Echt et al. studied the effects of prolonging time-to-therapy. (D. Echt, J. T. Barbey, J. N. Black, Influence of Ventricular Fibrillation Duration on Defibrillation Energy in Dogs Using Bidirectional Pulse Discharges, 11 PACE No. 9, 1315, Sep. 1988.) The results of this study indicate that the energy requirement for an efficacious defibrillation shock at thirty seconds of ventricular fibrillation is significantly greater than at five seconds of fibrillation.
Although previously known devices increase the therapeutic shock energy after failed attempts, they do not adjust the therapeutic shock energy to a greater value after the time-to-therapy has exceeded a predetermined or calculated critical time. Previously known devices also do not compensate for delays in administering therapy caused by inherent device characteristics. In addition, current devices do not provide a way of forecasting the time-to-therapy in order to set an appropriate energy value in advance of a cardiac event.
What is needed, therefore, is an automatic implantable cardiac stimulating device that forecasts the time delay between the onset of a tachyarrhythmia episode and the delivery of therapy. The device should determine the need for an increased energy shock on the basis of a comparison between a forecasted time-to-therapy and a predetermined critical time. In addition, an implantable cardiac stimulating device is needed that determines an actual elapsed time-to-therapy (i.e., from the initial onset of an arrhythmia to the time a therapeutic shock is delivered) and compares that elapsed time-to-therapy with the critical time to determine if an increased energy shock is required.